ANAESTHESIA FOR E.C.T

DR .A RAMAKRISHNA RAO

ASSISTANT PROFESSOR

Dept. of Anaesthesiology and Critical Care

Osmania Medical college

HISTORY 1500 AD – PARCELSUS induced seizures with

oral camphor to treat psychiatric illness.

1785 AD - 1st published report of the use of seizure – induced to treat mania , by using camphor.

1934 AD – VON MEDUNA of BUDAPEST (HUNGARY) began the modern era of convulsion therapy , using I.M injection of camphor for catatonic schizophrenia , quickly switched over to i.v pentylene tetrazole .

1938 AD – CERLETTI & BINI induced the convulsions electrically in a catatonic patient & produce a successful treatment response ( at ROME in April 1938).

1940 AD – BENNET used curare before its use in anaesthesia, to modify cardiazol induced convulsions.

ECT was introduced in the United States .

1948 AD – HUGUENARD & BOUE employed gallamine for ECT in 1948.

1951 AD – Introduction of succinylcholine for modified ECT , by HOLMBERG , THESLEFF & WONDERDEL of STOCKHOLM.

1957 AD – Hexafluorodiethyl ether was introduced to induce seizures by administering as vapour/gas.

1958 AD – First controlled study of unilateral E.C.T.

1960 AD – OTTOSSON demonstrated that attenuation of seizure with lidocaine reduced efficacy of E.C.T.

Comparision of neuroleptics versus E.C.T showed that neuroleptic is superior for acute treatment , although E.C.T may be more effective , in long term.

1970 AD – D ‘ELIA developed most common electrode positioning for right unlilateral E.C.T ( non-dominant electrode placement used to minimise retrogade amnesia after E.C.T)

1976 AD – A constant current BRIEF PULSE E.C.T device was developed.

1978 AD – The American Psychiatric association published the 1st task force report on E.C.T

1988 AD – Randomised controlled trials of E.C.T versus LITHIUM demonstrated them to be equally effective in treating MANIA.

2000 AD – high dose Rt. unilateral & bilateral E.C.T showed equal response rates in major depression .

Rt. unilateral electrode placement is associated with fewer

adverse cognitive effects.

Supreme court of India has given directions to all mental hospitals in India to administer only modified E.C.T & under Anaesthesia care .

INDICATIONS: Depression with suicidal tendencies , mood

disorders.

Catatonic schizophrenia

Mania when unmanageable

Psychosis – antepartum , postpartum

Refractory cases who are not responding to medication.

Indications (cont…) Rarely patients with mental retardation with psychosis

Geriatric patients with depression

- difficult to manage with drugs

. Schizoaffective disorders

Unipolar & Bipolar psychotic depression including mixed episodes.

OTHER INDICATIONS :

- Parkinson’s disease( to ↓ rigidity and bradykinesia)

- Neuroleptic malignant disorder

- For rapid definitive response

required on medical or psychiatric grounds

- Risk of alternative treatment outweigh benefits

- Past history of poor response to psychotropic or good response to E.C.T

- Patient preference

CONTRAINDICATIONS: ABSOLUTE:

Conditions associated with raised ICT(brain tumours and other SOL ‘s)

Recent MI of less than 3 months duration

Recent CVA of less than 3 months duration

RELATIVE:

Angina pectoris CHF Pheochromocytoma Glaucoma Retinal detachment Severe osteoporosis Major bones fracture High risk pregnancy Aneurysm of major vessel

PHYSIOLOGICAL CHANGES OCCURING DURING E.C.T ELECTRO PHYSIOLOGICAL PRINCIPLE :

PET ( POSITRON EMISSION TOMOGRAPHY)

Studies of both CBF and glucose uptake have shown during seizure that there is INCREASE in

- CBF - Uptake of glucose- Utilisation of oxygen- Permeablity of BBB( blood brain barrier)

Virtually every neurotransmitter is affected by E.C.T

A series of E.C.T sessions result in:

-down regulation of post synaptic ẞ - adrenergic receptors - ↑ in the post synaptic serotonin receptors- Affect the changes in the muscarinic ,

cholinergic and dopaminergic neuronal system.

Affect the coupling of the G proteins to the receptors , the activity of adenyl cyclase ,

phospho lipase ‘c’ and the regulation of the

Ca ++ entry into the neurons

ELECTRO PHYSIOLOGICAL PRINCIPLE OF E.C.T:

The normal brain activity is desynchronised , i.e neurons fire action potentials asynchronously

A convulsion or seizure occurs when a large percent of neurons fire in unison & propagate the seizure activity across the cortex and into the deeper structures and eventually engulf the entire brain in high voltage synchronous neuronal firing.

The cellular mechanisms work to contain the seizure activity and to maintain cellular homeostasis and seizure eventually ends .

In E.C.T the seizure activity triggered even in normal neurons .

MICROSCOPIC CHANGES AFTER E.C.T

Studies in rodents showed :

- Synaptic plasticity in hippocampus- Mossy fibre sprouting- Alterations in cytoskeletal structures- Increased connectivity in perforant pathways- The promotion of neurogenesis- The suppression of apoptosis

C.V.S EFFECTS OF E.C.T:

Parasympathetic outflow increases immediately after electrical stimulus , unopposed by anti-cholinergic premedication , sinus bradycardia , even brief clinically insignificant asystole can occur .

Supraventricular ectopic beats , atrial, junctional,nodal rhythm can occur. Atrial fibrillation , atrial flutter can be seen.

Following parasympathetic , sympathetic outflow increases mainly during electrical stimulation & post-ictally when adrenal gland releases catecholamines.

H.R , B.P , RPP increases which peaks immediately post-ictally & drops to pre E.C.T values within a minute ( may take 1 hr in older people > 50 yrs of age )

Hypertensive response may necessitate treatment with Trimethaphan , SNP, beta blocker (labetalol,esmolol), in some individuals Hydralazine , topical NTG.

T wave changes , ST depression can occur . Ventricular tachycardia , rarely VF .

Cardiac stabilization before E.C.T in cardiac pts necessary .Using lowest possible current during E.C.T

Pts with pacemaker , transplanted hearts are not contra -indications for E.C.T

RESPIRATORY SYSTEM : Exacerbation of underlying pulmonary

disease(asthma,COPD) Excess secretions Aspiration Negative pressure pulmonary edema

(inspiration against an obstructed airway or mechanical irritation precipitating laryngospasm)

Or pulmonary edema may be neurologically induced as a complication of status epilepticus

Sleep apnea syndrome may even be discovered during E.C.T anaesthesia (preoxygenation & nasopharyngeal airway , LMA will help).

Succinyl apnea due to prolonged hydrolysis of Suxamethonium due to pseudo-cholinesterase deficiency or concomitant drug therapy which interferes with suxamethonium hydrolysis.

C.N.S:

Blood flow to C.N.S increases

- ↑ O2 Consumption,↑ glucose uptake

- ↑ blood brain barrier permeability

Seizure induction leads to hyper-metabolic state

Post-ictally metabolic suppression develops

Current stimulates mood center in hypothalamus

Prolonged seizure (>3 min) may lead to structural brain injury with cardiovascular and pulmonary complications. (treat as status epilepticus )

▪Prolonged seizures are more common in the presence of pro-convulsant medications (theophylline , lithium , trazadone ) & in patients with h/o epilepsy and electrolyte imbalance.

DENTAL:

Unstable tooth may be broken / dislodged due to direct stimulation of jaw muscles.

MUSCULOSKELETAL:

Fractures of long bones , vertebrae , in 10% pts (during pre muscle relaxant era ) as a consequence of unmodified movements associated with seizure induction and expression

In osteoporotic pts , full paralytic dose of muscle relaxant is used for E.C.T treatment

Myalgias (due to depolarising muscle relaxant )

NEUROCOGNITIVE:

Post E.C.T disorientation , diminished processing of speech , decreased anterograde and retrograde memory, errors in visuo-spatial function , difficulty in word finding.

Use of lithium , drugs with anticholinergic effects aggravate cognitive impairment after E.C.T

Adverse cognitive effects can be attenuated by use of

N- METHYL D-ASPARTATE antagonists such as ketamine anaesthesia , thyroid hormones Post-ictal agitation , headache ,nausea.

NSAIDS(ketorolac) , triptans for migraine pts , in pts with nausea dopamine antagonist (compazine ) or 5 HT Antagonists (ondansetron ) are useful .

ECT MACHINES Brief pulse E.C.T machine

Sine wave E.C.T machine

current (800 milli amp) is fixed

Impedance check is present

Cognitive function is intact

Recovery smooth

Continuous flow of current , voltage & duration to be set

60-120 volt commonly used for a period of 0.6-1.2 sec

No impedance check Derranged cognition Bizzare recovery

PRE ANAESTHETIC EVALUATION(PAC)

GOALS : To reduce anxiety and counsel pt about

anaesthesia and E.C.T. Obtain full medical history of HTN , DM ,

Br.asthma , BPH , glaucoma , epilepsy , recurrent MI, porphyrias, OP poisoning , multiple fractures (trauma), substance abuse.

To perform detailed physical examination.

GENERAL EXAMINATION : PT should be examined thoroughly

Focus on cardiac , pulmonary , neurological systems

In a patient with catatonic schizophrenia

- G.C is poor , poor intake of food &fluids , -ve N2 balance , wasting , dehydration , may be on ryle ‘s tube feed , i.v feeding , foley ‘s catheter , may be semicomatose , do not respond to verbal commands & assumes a statue like posture

Mania pts:

-Well dressed , talkative , sometimes highly voilent and unmanageable .

Depression with suicidal tendencies

-calm and quite , express wish to die

GENERAL EXAMINATION: BP, temperature , P.R, R.R , are recorded

EXAMINATION OF ORAL CAVITY: For loose teeth , dentures , gingivitis , (phenytoin

therapy) Oral thrush , pyorrhoea , etc HIV , multiple drug abuse – oral thrush is commonly

seen Descending infection from oropharynx to lower

respiratory tract may be present .(clinical examination of lungs)

Neck movements , TMJ joint movements , to be tested

Look for any musculo skeletal disorders kyphosis , scoliosis , poliomyelitis , myasthenia gravis , etc to be ruled out

DRUG HISTORY EFFECTS OF CONCOMITANT THERAPY : Benzodiazepines , sodium valproate , carbamazepine

, phenytoin , etc - withdrawn before E.C.T for their anticonvulsant property.

LITHIUM – may cause post-ictal delirium , prolongs seizure activity , may interact with neuromuscular blocking agents

CLOZAPINE , BUPROPION – withdrawn before E.C.T because of the property of late appearing seizure , extrapyramidal symptoms , involuntary movements , tardive dyskinesia .

Lidocaine should not be administered during E.C.T , because it increases the seizure threshold.

Theophylline contraindicated – because it increases the duration of seizure

Chlorpromazine , haloperidol , promethazine , may decrease cardiac output & cause hypotension . They cause baseline sedation (↓ anaesthetic dose considerably )

Newer antipsychotic drugs such as olanzapine known to cause D.M , & weight gain abnormally .

Venlaflaxin , an antidepressant , is known to cause HTN in normotensives

Other drug interactions with MAIO’s , (isocarboxazid,phenelzine,tranylcypromine), TCA’s ,(amitriptyline , amoxapine,desiprimine , doxepin , imipramine , maprotiline,nortrityline , protryptiline , trimipramine ) to be remembered(advised to discontinue before ECT)

Known h/o pseudocholinesterase deficiency- suxamethonium apnea – may necessitate endotracheal intubation

Pt with history of previous exposure to anaesthesia , E.C.T earlier and was it uneventful or not , to be noted.

Any prolonged recovery from NM block & delayed recovery to be noted .

Antihypertensives , beta blockers (can enhance bradycardia, precipitate asystole )

Labetalol , esmolol are better agents during E.C.T therapy.

Diuretics , oral hypoglycemics , insulin can be continued .

Remember , long acting anticholinesterase use (ECHOTHIOPATE) for pts with glaucoma causes delayed recovery from suxamethonium

Caffiene – can ↑ the seizure duration. Lithium – may cause post-ictal confusion ,

serotonin syndrome , prolonged seizures . Quitiapine – has anti convulsant property

and reduces the efficacy of ECT. Antipsychotic that has to be stopped

before ECT is – RESERPINE TCA’s & serotonin reuptake inhibitors

increase seizure duration .

INVESTIGATIONS: CBP , ESR , X – ray chest PA view , ECG , blood sugar , blood

urea , urine analysis , electrolyte estimation , thyroid profile ,& pregnancy tests in women

Any clinical features of raised ICT , & look for direct opthalmoscopy ( fundoscopy) to rule out raised ICT .

CT scan , MRI may help to clinch diagnosis.

Testing of plasma pseudocholinesterase or DIBUCANINE number in family history of pseudocholinesterase deficiency.

In pts with skeletal injury or disease spine x-rays are advised.

CONSENT

Consent of mentally ill pt & its validity in the court of law is questionable .

Written informed consent from pt & legally sanctioned surrogate .

Consent can include both the anaesthetic procedure & electrical stimulation (ECT) or separate consent form for two procedures

Take the signature of the witness if necessary.

ADMISSION UNDER SPECIAL CONDITIONS : 2 separate psychiatrists will examine the pt

independently & arrive to a conclusion that the individual requires treatment and hospitilization – in the interest of pt, ECT can be performed .

When the pt is brought to hospital with reception order from judicial 1st class magistrate for treatment & report , in this case consent is deemed to be conferred by the court .

ANAESTHESIA MANAGEMENT OF ECT

Identify the pt by staff & relatives Photo identity of mentally ill pt is advisable

. Confidentiality is very important Photo identity is useful in case of escape

of pt. NBM for 6 hours Most psychotropic drugs can cause delay

in gastric emptying & dryness of mouth

Enema , catheterisation of bladder not necessary.

(pt is advised to void urine before brought into ECT suite) Female pts advised to remove jewellery,

lipstick smear , nail polish (likely to hinder monitoring of oxygenation )

They should wear loose garments to facilitate free respiratory movements

ELECTRODE PLACEMENT:

Bifronto-temporal electrode placement commonly practiced

ECT devices in the US are restricted to an output in the range of 504-576 mc.

stimulus wave form – a bipolar rectangular pulse with 0.5 – 2 ms wide .

SEIZURE THRESHOLD AND DOSING : Normally 8-12 times of seizure threshold is

given as dose. Adequate seizure duration was also postulated

to be necessary for therapeutic response . (duration of 30 – 120 secs advised for efficacy

of E.C.T) Seizure of < 20 secs not effective

therapeutically . The facilities should be like in any standard OT

with monitoring facilities .

MONITORING

Cardiac monitoring

Pulse oximetry

NIBP (set at short frequency)

2 lead EEG monitoring (monitoring necessary at US standards )

PROCEDURE

MODIFIED ECT: Venous access is secured Inj . Atropine 0.6mg i.v (seperately or mixed

with induction agent ) Inj . Thiopentone sodium 3-4 mg / kg 2.5%

solution slowly , sleep dose by titration .

Ideal agent in E.C.T provides rapid onset , short duration, rapid recovery , no adverse shortening of seizure duration .

Alternatively , if barbituates are contraindicated use 1% propofol , 1.5mg/kg

Propofol- no convulsant or anti convulsant properties , no marked interactions with TCA ’s , MAOI , early orientation , antiemetic property

Ideally Methohexitone is prefered over TPS because TPS is associated with post-ictal arrythmias , longer recovery period , TPS also acts as better anticonvulsant than Methohexitone.

Methohexitone is better than TPS in cardiac patients

Althesin , Propanidid , were also used as hypnotics but have high incidence of Anaphylactoid / Anaphylactic reactions and

prolong the action of Suxamethonium.

Diazepam ↑ seizure threshold & shortens seizure duration .

ECG changes are higher with Diazepam than with Methohexitone .

Electrical stimulus is applied bitemporally after keeping a mouth gag / mouth prop with median slit in between the teeth to prevent tongue biting .

The buccal mucosa is seperated from the teeth edges to avoid soft tissue injury

Once the tonic clonic movements subside , the oral cavity is thouroughly sucked out & the pt is ventillated with O2 by positive pressure till recovery from neuro muscular blocking agent .

care should be exercised while using barbituates as they may cause depression of cardiac output , ↓ cerebral perfusion pressure , CVS collapse , respiratory depression which may necessitate c/v

In patients with hepatic dysfunction , TPS dose is ↓ considerably as it is metabolized in the liver

There is a pilomotor reaction & pupillary dilation after the electrical stimulus . Conjunctival suffusion , goose pimples are observed . Flushing of facial skin is seen

DIFF B/W MODIFIED & DIRECT ECTMODIFIED DIRECT

Smooth induction and abrupt recovery

Succinyl apnea may be possibility

Muscles are well relaxed and fine jerky movements observed

Fractures and dislocations are rare & minimal

Smooth induction and delayed recovery

No succinyl apnea

Vigorous jerky movements

Fractures and dislocations may occur , loose teeth may dislodge

MODIFIED DIRECT

Respiration has to be assisted immediately after ECT till spont. vent is established

Respiration established with initial hyperventillation , muscular spasm is quite common . Mouth gag with median slit is useful for suction .

AWAKE ECT

INDICATIONS : Patients with general condition very poor

, other biochemical parameters are highly deranged , increased anaesthesia risk , pts who might commit suicide without ECT treatment .

Only inj .atropine / glycopyrrolate is given

Pts are oxygenated thouroughly and administered ECT . However the outcome of ECT is good in such pts.

An immediate loss of consciousness with the passage of electric current .

A tonic convulsion for 5 secs leading to a clonic convulsion with regular muscle movement lasting for 10-15 secs .

Direct stimulation of the muscle fibres by electric current cause contraction of jaw muscles .

POST E.C.T CARE AND COMPLICATIONS :

Staff nurse to look after the patient’s condition

- pulse oximetry

- suction apparatus

- bed side O2 supply Attendánt may be allowed to be with the

patient

AFTER E.C.T: Shift the pt on a trolley to the bed , keep in

lateral position , keeping the neck in extended position to ease the airway & trickle out any left over secretions .

Look for respiratory movements Usually patient recovers over a period of ½ hr Incidence of tongue fall leading to upper airway

obstruction , ( bradycardia , hiccups , cyanosis ) . An oro pharyngeal airway may be necessary in some cases

OTHER IMPORTANT COMPLICATIONS AFTER ECT: Suxamethonium apnea

(support respiration with controlled ventilation with mask/ET tube )

Bronchospasm , laryngospasm ( treat immediately )

Iatrogenic – ECT induced

Post-ictal stiffening ( board like rigidity of the whole body)

Post-ictal amnesia/ confusion / agitation

Status asthamaticus Status epilepticus Postural hypotension OP poisoning cases posted for modified

ECT

- SUCCINYL APNEA , PULMONARY EDEMA , DEATH Risk of death – 1:10,000 in modern

population undergoing ECT ( cardiac complication is most common cause )

CONCLUSION Anaesthesia for ECT looks like a simple short

procedure , it has to be tackled effectively to contain all the possible problems mentioned previously .

(one death reported in TEXAS (USA) due to laryngospasm) It should be well equipped with all

armamentarium in the OT to tackle any eventuality.

3rd trimester pregnancy – pt is intubated and wedge placed under rt hip .

REFERENCES

KAPLAN & SADOCK ’ S “ COMPREHENSIVE TEXT BOOK OF PSYCHIATRY”

ANAESTHESIA – RONALD MILLER VOL 2 , 3RD EDITION, 6th EDITION

WYLIE – CHURCHIL DAVIDSON – PRACTICE OF ANAESTHESIA 5TH EDITION

LEE ’S SYNOPSIS – 12TH EDITION

Thank you